Molecular Genetics of Cardiac Electrophysiology

  • Charles I. Berul
  • Jeffrey A. Towbin

Part of the Developments in Cardiovascular Medicine book series (DICM, volume 231)

Table of contents

  1. Front Matter
    Pages i-xiii
  2. Overview: Genetics of Cardiac Electrophysiology

    1. Jeffrey A. Towbin, Charles I. Berul
      Pages 1-2
  3. Experimental Investigation of Inherited Electrophysiological Disorders

    1. Coeli M. B. Lopes, Steve A. N. Goldstein, Michael Apkon
      Pages 3-21
    2. Amit Rakhit, Charles I. Berul
      Pages 23-44
    3. Gregory E. Morley, Dhananjay Vaidya, José Jalife
      Pages 45-60
    4. Deborah L. Lerner, Jeffrey E. Saffitz
      Pages 61-80
  4. Hereditary Arrhythmias

    1. Patrick Y. Jay, Charles I. Berul
      Pages 81-91
    2. Ramon Brugada, Robert Roberts
      Pages 93-100
    3. Robert M. Hamilton
      Pages 101-118
  5. Ion Channel Mutations with Clinical Electrophysiologic Consequences

    1. G. Michael Vincent, Katherine Timothy
      Pages 119-135
    2. Jeffrey A. Towbin, Matteo Vatta, Koonalee Nademanee, Ramon Brugada, Josep Brugada, Charles Antzelevitch et al.
      Pages 147-180
  6. Inherited Cardiomyopathies with Arrhythmias

    1. Laura M. Bevilacqua, Charles I. Berul
      Pages 181-194
    2. Jeffrey A. Towbin, Neil E. Bowles
      Pages 195-218
    3. Mira Irons, Ellen Roy Elias
      Pages 219-237
    4. Frank I. Marcus, Peter Ott
      Pages 239-250
    5. Sita Reddy, Charles I. Berul
      Pages 267-286
  7. Inherited Structural Heart Diseases Associated with Arrhythmias

    1. Kristen Patton, Christine E. Seidman
      Pages 287-296
    2. Cathy J. Hatcher, Craig T. Basson
      Pages 297-315

About this book

Introduction

The molecular basis for atrial fibrillation continues to be largely unknown, and therapy remains unchanged, aimed at controlling the heart rate and preventing systemic emboli with anticoagulation. Familial atrial fibrillation is more common than previously suspected. While atrial fibrillation is commonly associated with acquired heart disease, a significant proportion of individuals have early onset without other forms of heart disease, referred to as "lone" atrial fibrillators. It is also well recognized that atrial fibrillation occurs on a reversible or functional basis, without associated structural heart disease, such as with hyperthyroidism or of atrial fibrillation following surgery. It remains to be determined what percentage in these individuals is familial or due to a genetic predisposition. Mapping the locus for familial atrial fibrillation is the first step towards the identification of the gene. Isolation of the gene and subsequent identification of the responsible molecular genetic defect should provide a point of entry into the mechanism responsible for the familial form and the common acquired forms of the disease and eventually provide more effective therapy. We know that the ionic currents responsible for the action potential of the atrium is due to multiple channel proteins as is electrical conduction throughout the atria. Analogous to the ongoing genetic studies in patients with familial long QT syndrome, it is highly likely that defects in each of these channel proteins will be manifested in familial atrial fibrillation.

Keywords

arrhythmia atrial fibrillation cardiology electrophysiology genetics heart heart disease physiology

Editors and affiliations

  • Charles I. Berul
    • 1
    • 2
  • Jeffrey A. Towbin
    • 3
  1. 1.Department of CardiologyChildren’s HospitalBostonUSA
  2. 2.Department of PediatricsHarvard Medical SchoolBostonUSA
  3. 3.Departments of Pediatrics (Cardiology), Molecular and Human GeneticsTexas Children’s Hospital, Baylor College of MedicineHoustonUSA

Bibliographic information

  • DOI https://doi.org/10.1007/978-1-4615-4517-0
  • Copyright Information Kluwer Academic Publishers 2000
  • Publisher Name Springer, Boston, MA
  • eBook Packages Springer Book Archive
  • Print ISBN 978-1-4613-7037-6
  • Online ISBN 978-1-4615-4517-0
  • Series Print ISSN 0166-9842
  • About this book